1. Field of the Invention
The present invention relates to a method and system for restoration and repair of a body joint, such as the knee.
2. Background Art
Articular cartilage and meniscal cartilage provide the mobile weight bearing surfaces of the knee joint. Damage to these surfaces is generally due to genetic predisposition, trauma, and/or aging. The result is usually the development of chondromalacia, thinning and softening of the articular cartilage, and degenerative tearing of the meniscal cartilage. Various methods of treatment are available to treat these disease processes. Each option usually has specific indications and is accompanied by a list of benefits and deficiencies that may be compared to other options.
Especially in the case of early onset osteoarthritis, the destruction of the articular material is generally localized to specific areas on the femoral condyle and tibial plateau. It is rarely widespread and often lacking the presence of eburnated bone. As the disease progresses, the damage to the articular material increases and patches of exposed bone may appear, with the area of degeneration typically being irregularly shaped and of varying depth. At this stage, it is often common to see the formation of osteophytes along the periphery of the tibial plateau and femoral condyle in response to the increased localized loading due to the disease changing the shape of the articulating members (FIGS. 1a and 1b).
The healthy knee joint has a balanced amount of joint cartilage across the four surfaces of this bicompartmental joint (medial femoral condyle, medial tibial plateau, lateral femoral condyle, and lateral tibial plateau). In patients with osteoarthritis, the degenerative process typically leads to an asymmetric wear pattern that leaves one compartment with significantly less articular cartilage covering the distal portions (or weight bearing area) of the tibia and femur than the other compartment. Most commonly, the medial compartment of the knee joint is affected more than the lateral compartment.
As the disease progresses, large amounts of articular cartilage are worn away. Due to the asymmetric nature of the erosion, the alignment of the mechanical axis of rotation of the femur relative to the tibia becomes tilted down towards the compartment which is suffering the majority of the erosion. The result is a varus (bow-legged) deformity in the case of a medial compartment disease predominance, or a valgus (knock-kneed) deformity in the case of lateral compartment disease predominance. Factors such as excessive body weight, previous traumatic injury, knee instability, the absence of the meniscus, and genetic predisposition all affect the rate of the disease.
Osteoarthritis is usually defined in stages of Grade I through V, with Grade III revealing significant articular cartilage loss, Grade IV revealing some eburnation of the subchondral bone, and Grade V detailing both significant articular loss and bone loss. The disease manifests itself as periodic to continuous pain that can be quite uncomfortable for the patient. The cause of this pain is subject to many opinions but it is apparent that, as the joint compartment collapses, the collateral ligament on the side of the predominant disease becomes increasingly slack (like one side of a pair of loose suspenders), and the tibial and femoral axes move, for example, from a varus to a valgus condition. This increases the stress on the opposing collateral ligament as well as the cruciate ligaments, and shifts the load bearing function of this bicompartmental joint increasingly towards the diseased side. This increasing joint laxity is suspected of causing some of the pain one feels. In addition, as the bearing loads are shifted, the body responds to the increased loading on the diseased compartment with an increased production of bony surface area (osteophytes) in an attempt to reduce the ever-increasing area unit loading. All of this shifting of the knee component geometry causes a misalignment of the mechanical axis of the joint. This misalignment causes an increase in the rate of degenerative change to the diseased joint surfaces, causing an ever-increasing amount of cartilage debris to build up in the joint, and further causing joint inflammation and subsequent pain.
Currently, there is a void in options used to treat the relatively young patient with moderate to severe chondromalacia involving mainly one compartment of the knee. Current treatments include NSAIDS, cortisone injections, hyaluronic acid (HA) injections, and arthroscopic debridement. Some patients cannot tolerate or do not want the risk of potential side effects of NSAIDS. Repeated cortisone injections actually weaken articular cartilage after a long period of time. HA has shown promising results, but is only a short term solution for pain. Arthroscopic debridement alone frequently does not provide long lasting relief of symptoms.
Unfortunately, the lack of long term success of these treatments leads to more invasive treatment methods. Osteochondral allografts and microfracture techniques are indicated for small cartilage defects that are typically the result of trauma. These procedures are not suitable for addressing large areas of degeneration. In addition, osteochondral allografts can only be used to address defects on the femoral condyle, as tibial degeneration cannot be addressed with this technique. High tibial osteotomy (HTO) corrects the varus malalignment between the tibia and the femur but, because it is performed below the joint line, it does not fill the cartilage void or re-tension the medial collateral ligament (MCL). Removing bone and changing the joint line complicates the conversion to total knee arthroscopy (TKA). In addition, an HTO does leave a hard sclerotic region of bone which is difficult to penetrate, making conversion to a total knee replacement (TKR) technically challenging.
Currently, patients with large joint defects require replacement of the existing surfaces with materials other than articular cartilage. This is only possible with a primary (first arthroplasty performed on the joint) total (TKR) or uni-condylar (UKR) knee replacement. These procedures require the resection of significant amounts of the underlying bone structure; typically 7-9 mm. Primary procedures have typical functional life spans of 5-15 years, and thus younger patients undergoing this procedure will likely require revision (secondary) surgery as they age. However, the amount of bone loss that is inherent in these procedures makes a revision procedure much more difficult in the future as even more bone must be removed. Revision total knee replacement surgery is usually extensive and results in predictably diminished mechanical life expectancy. Therefore, it is best to delay this type of bone resecting surgery as long as possible.
Treatments such as osteochondral transplants (OATS procedure) fill defects with a series of small transplanted plugs of bone and cartilage. Metallic plugs, such as those described in U.S. Pat. Nos. 6,520,964 and 6,610,067, have also been used in an attempt to repair smaller defects in the tibial or femoral surfaces. Larger defects, such as avascular necrosis (AVN) are typically treated with donor (cadaver) allografts. Both methods have achieved limited success, as neither method is able to completely transition from the repaired defect area to the surrounding healthy areas without the creation of localized areas of high stress concentration, leading to premature failure.
Mobile prostheses may be implanted to attempt to restore joint function in the osteoarthritic patient. Such prostheses are typically designed to move over a relatively flat, smooth joint surface during the patient ROM. However, in the typical, moderately diseased osteoarthritic patient, the subchondral bone of both the plateau and condyle have become somewhat remodeled and reshaped due to the eccentric loading of the medial compartment. Once the prosthesis is implanted, there may be further “reshaping” of these bearing surfaces as well as the underlying bony structure until their geometries are conformal with the prosthesis shape, thereby possibly leading to pain. Once the joint is realigned to a neutral or valgus condition, the soft tissue, which has tolerated the varus alignment for so many years, may be painfully stressed into this new alignment. Only under-correction of the alignment would prevent this occurrence, but this option would leave joint instability for the patient.